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ID 119239
タイトル別表記
sPLA2- IID, an Immunosuppressive sPLA2
著者
Miki, Yoshimi Tokyo Metropolitan Institute of Medical Science
Kidoguchi, Yuh Tokyo Metropolitan Institute of Medical Science|Tokyo Denki University
Sato, Mariko Tokyo Metropolitan Institute of Medical Science|Tokyo Denki University
Taketomi, Yoshitaka Tokyo Metropolitan Institute of Medical Science
Taya, Choji Tokyo Metropolitan Institute of Medical Science
Muramatsu, Kazuaki Tokyo Denki University
Gelb, Michael H. University of Washington
山本, 圭 Tokyo Metropolitan Institute of Medical Science|Tokushima University|Japan Agency for Medical Research and Development 徳島大学 教育研究者総覧 KAKEN研究者をさがす
Murakami, Makoto Tokyo Metropolitan Institute of Medical Science|Japan Agency for Medical Research and Development
資料タイプ
学術雑誌論文
抄録
Phospholipase A2 enzymes have long been implicated in the promotion of inflammation by mobilizing pro-inflammatory lipid mediators, yet recent evidence suggests that they also contribute to anti-inflammatory or pro-resolving programs. Group IID-secreted phospholipase A2 (sPLA2-IID) is abundantly expressed in dendritic cells in lymphoid tissues and resolves the Th1 immune response by controlling the steady-state levels of anti-inflammatory lipids such as docosahexaenoic acid and its metabolites. Here, we show that psoriasis and contact dermatitis were exacerbated in Pla2g2d-null mice, whereas they were ameliorated in Pla2g2d-overexpressing transgenic mice, relative to littermate wild-type mice. These phenotypes were associated with concomitant alterations in the tissue levels of ω3 polyunsaturated fatty acid (PUFA) metabolites, which had the capacity to reduce the expression of pro-inflammatory and Th1/Th17- type cytokines in dendritic cells or lymph node cells. In the context of cancer, however, Pla2g2d deficiency resulted in marked attenuation of skin carcinogenesis, likely because of the augmented anti-tumor immunity. Altogether, these results underscore a general role of sPLA2-IID as an immunosuppressive sPLA2 that allows the microenvironmental lipid balance toward an anti-inflammatory state, exerting beneficial or detrimental impact depending upon distinct pathophysiological contexts in inflammation and cancer.
掲載誌名
Journal of Biological Chemistry
ISSN
00219258
1083351X
cat書誌ID
AA1202441X
出版者
American Society for Biochemistry and Molecular Biology|Elsevier
291
30
開始ページ
15588
終了ページ
15601
発行日
2016-05-21
権利情報
This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
EDB ID
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
生物資源系